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diagnosed with grade II fibrosarcoma in the thigh and left-scapular region in November 1999&#46; Tumour resection was indicated&#46;</p><p class="elsevierStylePara">Three years later&#44; he developed progressive pulmonary metastatic disease&#44; which was treated with surgery and chemotherapy &#40;MAID protocol&#58; mesna&#44; adriamycin&#44; ifosfamide and dacarbazine&#41;&#46;</p><p class="elsevierStylePara">In May 2004&#44; he developed progressive pulmonary metastatic disease again and was treated with taxotere and gemcitabine&#44; completing 6 cycles&#46; He then completed 21 cycles of therapy with gemcitabine only&#46;</p><p class="elsevierStylePara">In August 2008&#44; he started gemcitabine and bevacizumab treatment&#44; due to a disease relapse&#46;</p><p class="elsevierStylePara">Following the second bevacizumab dosage&#44; the patient was admitted due to headache&#44; arterial hypertension &#40;AHT&#41; &#40;BP&#58; 190&#47;100mm Hg&#41; and general oedema&#46; Upon admission&#44; he had creatinine at 1&#46;8mg&#47;dl&#44; nephrotic-range proteinuria and microhaematuria&#46; Moderate normocytic&#47;normochromic anaemia without schistocytes on the peripheral blood smear&#46; Kidney ultrasound was normal&#46; Immunological study only had low C3 levels&#46; He had no previous history of AHT or kidney disease&#46;</p><p class="elsevierStylePara">On the sixth day of his hospital stay&#44; a renal biopsy was performed finding mesangiocapillary glomerulonephritis type II&#46;</p><p class="elsevierStylePara">Gemcitabine and bevacizumab treatment was suspended and angiotensin II receptor antagonist &#40;ARA-II&#41; treatment started&#46; Renal function improved&#44; finally reaching creatinine levels of 1&#46;1mg&#47;dl&#59; proteinuria decreased significantly and optimum blood pressure control was achieved&#46;</p><p class="elsevierStylePara">Proteinuria in anti-VEGF-treated patients has been related to damage in the podocyte-endothelial-VEGF axis&#46; VEGF production by podocytes is necessary for the glomerular endothelial to remain intact&#46;<span class="elsevierStyleSup">2</span> VEGF is expressed in the podocytes and its receptors are found in the endothelial cells of the normal glomerular capillaries&#46;<span class="elsevierStyleSup">3 </span>When VEGF binds to its receptor&#44; it promotes an increase in the microvasculature&#8217;s permeability&#44; cell migration and division&#44; apoptosis inhibition and endothelial damage repair&#46;<span class="elsevierStyleSup">4 </span></p><p class="elsevierStylePara">In animal studies&#44; a defect in the VEGF expression causes glomerular diseases characterised by nephrotic-range proteinuria&#44; endotheliosis and hyaline deposits&#44; which are similar to the kidney damage found in pre-eclampsia patients&#46;<span class="elsevierStyleSup">5 </span></p><p class="elsevierStylePara">We only found a few glomerulonephritis cases associated with anti-VEGF antibodies in the medical literature&#44; and most were thrombotic microangiopathies&#46; Bevacizumab-induced mesangiocapillary glomerulonephritis seems to be very rare&#46; We believe that more cases will gradually appear due to the increased use of these antibodies in oncology in recent years&#46;</p><p class="elsevierStylePara">Proteinuria which appears as a result of bevacizumab-induced glomerular damage seems to be reversible&#44; at least partially&#44; when this chemotherapy agent is suspended&#46;</p><p class="elsevierStylePara">Our case&#44; and other similar cases of patients with metastasis which develop bevacizumab-induced proteinuria had been treated with other&#44; potentially nephrotoxic agents&#46; Our patient also received high doses of gemcitabine over a long period of time&#46; Little is still known about gemcitabine&#8217;s mechanism of action on kidney damage&#44; although we know that it is dose-dependent&#46; In most cases&#44; it is associated with haemolytic uremic syndrome&#44;<span class="elsevierStyleSup">6</span> although we have also found isolated cases associated with mesangiocapillary glomerulonephritis&#46;<span class="elsevierStyleSup">7 </span></p><p class="elsevierStylePara">Given that a kidney biopsy was not performed before bevacizumab treatment&#44; we are not able to confirm that gemcitabine was not responsible for the patient&#8217;s symptoms&#46; However&#44; given that the kidney damage was not evident until the start of anti-VEGF antibody treatment&#44; we believe that the agent responsible for these symptoms was bevacizumab&#46; It is possible that gemcitabine treatment produces initial renal damage&#44; which may have been exacerbated by bevacizumab administration&#46;</p><p class="elsevierStylePara">We recommend a strict control of the arterial pressure and kidney function in patients undergoing monoclonal antibody therapies&#46;</p>"
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